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Abstract
Ranolazine is an agent approved for the symptomatic treatment of chronic stable angina that inhibits the late inward sodium current (INaL). INaL amplitude is increased under several pathological conditions, including increased oxidative stress, myocardial ischemia, cardiac hypertrophy, heart failure, long-QT syndrome variant 3 and atrial fibrillation. Experimental and preliminary clinical evidence suggests that ranolazine may represent a new therapeutic strategy in the treatment of a broad spectrum of cardiac arrhythmias. This article reviews the role of the INaL and provides an update on experimental and clinical evidence supporting the efficacy and safety of ranolazine across a broad spectrum of arrhythmias.
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Financial & competing interests disclosure
Funding was provided by grants from the Ministerio de Ciencia e Innovación (SAF2008-04903), the Instittuto de Salud Carlos III (PI080665 and Red HERACLES RD06/0009-FEDER), the Spanish Society of Cardiology and Centro Nacional de Investigaciones Cardiovasculares (CNIC-13). The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
No writing assistance was utilized in the production of this manuscript.
Notes
ATX-II: Anemonia sulcata toxin; CaMKIIδ: Calmodulin-dependent protein kinase IIδ; LV: Left ventricular; INaL: Late inward sodium current; Na+: Sodium.